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WIN55212-2通过调控akt/mtor/PFKFB3信号通路减轻脓毒症小鼠急性肾损伤

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陆军军医大学学报 2024年第10期46卷 1100-1106页

作者：董旭鹏段倩雯马源刘澈龚禹马玉清兰州大学第一临床医学院兰州730000 兰州大学第一医院麻醉科兰州730000

目的探讨大麻素受体激动剂WIN55212-2(WIN)对脓毒症小鼠急性肾损伤(acute kidney injury,AKI)的影响及其作用机制。方法24只雄性健康小鼠分为4组(n=6):对照组(Control组)、脓毒症组(LPS组)、脓毒症+WIN55212-2组(LPS+WIN组)和脓毒症+WIN55212-2+mtor激活剂MHY1485组(LPS+WIN+MHY组)。采用腹腔注射脂多糖(lipopolysaccharide,LPS)的方法构建脓毒症模型,造模24 h后取材,ELISA测定肾脏组织IL-1β、IL-18和乳酸脱氢酶A(lactate dehydrogenase A,LDHA)的含量以及血清Scr、肾损伤分子-1(kidney injury molecule-1,KIM-1)和乳酸的含量;HE染色观察肾脏组织病理改变并进行Paller评分,Western blot检测肾脏组织p-akt、p-mtor及6-磷酸果糖激酶-2/果糖-2,6-二磷酸酶3(6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3,PFKFB3)的表达。结果与Control组相比,LPS组HE染色显示肾脏组织受损,Paller评分升高(Pakt、p-mtor、PFKFB3表达增加(Pakt、p-mtor、PFKFB3表达减少(Pakt、p-mtor、PFKFB3表达增加(Pakt/mtor/PFKFB3信号通路,降低肾脏组织糖酵解水平,减轻炎症反应。

关键词：脓毒症急性肾损伤有氧糖酵解 akt/mtor

基于akt/mtor自噬通路介导NLRP3炎症小体失活探讨冲和膏促进糖尿病大鼠溃疡创面愈合的作用机制

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中药新药与临床药理 2024年第6期35卷 841-849页

作者：党赢师建平张锁刘钰海日吴昊焦雨琦王璐白洁陈旭内蒙古医科大学内蒙古呼和浩特010110

目的探讨冲和膏通过蛋白激酶B(akt)/哺乳动物雷帕霉素靶蛋白(mtor)自噬通路介导核苷酸结合寡聚酸结构域样受体蛋白3(NLRP3)炎症小体失活对糖尿病大鼠溃疡创面愈合的作用机制。方法采用高糖高脂饲料喂养、腹腔注射链脲佐菌素(Streptozoci... 详细信息

目的探讨冲和膏通过蛋白激酶B(akt)/哺乳动物雷帕霉素靶蛋白(mtor)自噬通路介导核苷酸结合寡聚酸结构域样受体蛋白3(NLRP3)炎症小体失活对糖尿病大鼠溃疡创面愈合的作用机制。方法采用高糖高脂饲料喂养、腹腔注射链脲佐菌素(Streptozocin,STZ)联合皮肤缺损方法构建糖尿病溃疡SD大鼠创面模型36只,将大鼠随机分为模型组、冲和膏组和生长因子组,每组12只。另取12只SD大鼠构建普通创面模型作为空白组。空白组和模型组不进行药物干预,冲和膏组和生长因子组分别外敷冲和膏、生长因子凝胶,观察记录各组大鼠创面愈合情况。给药第7天和第14天分别取材,HE染色观察创面组织病理学改变,并进行成纤维细胞计数;ELISA法检测血清中白细胞介素(IL)-1β、IL-18、肿瘤坏死因子(TNF)-α水平;免疫组化检测创面肉芽组织自噬相关蛋白Beclin-1、LC3-Ⅱ表达水平;Western Blot法检测创面肉芽组织炎症小体相关蛋白NLRP3、含Caspase募集结构域的凋亡相关斑点样蛋白(ASC)、Caspase-1、Pro-Caspase-1及akt/mtor自噬通路相关蛋白akt、p-akt、mtor、p-mtor的表达情况。结果与空白组比较,模型组在第7天和第14天创面病理损伤修复延缓,单位面积成纤维细胞数量较少(Pmtor、p-mtor、akt、p-akt表达水平降低(Pmtor、p-mtor、akt、p-akt表达水平升高(Pakt/mtor通路介导NLRP3炎症小体失活,改善创面自噬水平,从而促进糖尿病大鼠溃疡创面愈合。

关键词：冲和膏 akt/mtor NLRP3 糖尿病溃疡创面愈合自噬大鼠

石蒜碱调节akt/mtor信号通路对乳腺癌细胞曲妥珠单抗耐药的影响

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南开大学学报(自然科学版) 2024年第4期 79-85页

作者：杨芳沈国栋徐婷娟李瑞麟安徽医科大学第二附属医院妇产科安徽医科大学第二临床医学院中国科学技术大学附属第一医院&安徽省立医院老年医学科肿瘤免疫与营养治疗安徽省重点实验室安徽省老年医学研究所安徽医科大学第三附属医院药学部

石蒜碱具有显著的抗肿瘤活性,可增强顺铂对肝癌细胞敏感性及细胞毒性.本研究采用体外培养人乳腺癌细胞SKBR3,以5μg/mL的TZB连续给药诱导建立TZB耐药细胞SKBR3/TR,以CCK-8法筛选石蒜碱最佳作用浓度后检测其对SKBR3/TR细胞TZB耐药指数的... 详细信息

石蒜碱具有显著的抗肿瘤活性,可增强顺铂对肝癌细胞敏感性及细胞毒性.本研究采用体外培养人乳腺癌细胞SKBR3,以5μg/mL的TZB连续给药诱导建立TZB耐药细胞SKBR3/TR,以CCK-8法筛选石蒜碱最佳作用浓度后检测其对SKBR3/TR细胞TZB耐药指数的影响.构建SKBR3/TR移植瘤裸鼠模型,随机分为对照组、TZB组、TZB+石蒜碱组,药物干预后检测各组裸鼠肿瘤体积与质量.将体外培养的SKBR3/TR细胞随机分为对照组、TZB组、TZB+SC79组、TZB+石蒜碱组、TZB+石蒜碱+SC79(akt激活剂)组,药物分组干预后以免疫印迹实验检测akt/mtor信号通路相关蛋白表达;以流式细胞实验、CCK-8法、结晶紫染色分别检测各组细胞凋亡和增殖;以免疫印迹实验检测各组细胞增殖(PCNA)、凋亡(Bax、Cleaved Caspase-3、Bcl-2)及耐药P-糖蛋白(P-gp)相关蛋白表达.探讨石蒜碱调节akt/mtor信号通路对乳腺癌细胞曲妥珠单抗(TZB)耐药的影响.结果显示:石蒜碱可明显降低SKBR3/TR细胞TZB耐药指数,并增强TZB对SKBR3/TR移植瘤裸鼠肿瘤生长的抑制作用.与对照组、TZB组相比,TZB+石蒜碱组细胞的凋亡率、Bax与Cleaved Caspase-3蛋白表达升高(Pakt/akt、p-mtor/mtor、细胞活力、集落形成率、PCNA与Bcl-2、P-gp蛋白表达降低(Pakt/mtor信号通路激活,从而减轻乳腺癌细胞的TZB耐药性.

关键词：石蒜碱 akt/mtor 乳腺癌曲妥珠单抗耐药

LncRNA TUG1靶向akt/mtor信号通路促进卵巢癌细胞增殖和转移的研究

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实用癌症杂志 2024年第6期39卷 883-886页

作者：蔡阳阳吴向晖熊丽丽河南科技大学第一附属医院 471000

目的探究长链非编码RNA牛磺酸上调基因1(lncRNA TUG1)通过介导蛋白激酶B/磷酸化哺乳动物雷帕霉素靶蛋白(akt/mtor)信号通路对卵巢癌细胞增殖和转移的影响及可能机制。方法收集112例行卵巢癌根治术患者的卵巢癌组织及癌旁组织,采用RT-PC... 详细信息

目的探究长链非编码RNA牛磺酸上调基因1(lncRNA TUG1)通过介导蛋白激酶B/磷酸化哺乳动物雷帕霉素靶蛋白(akt/mtor)信号通路对卵巢癌细胞增殖和转移的影响及可能机制。方法收集112例行卵巢癌根治术患者的卵巢癌组织及癌旁组织,采用RT-PCR检测两组织、卵巢癌细胞(OC3,SKOV3,A2780,HO-8910)及人正常卵巢上皮细胞IOSE80中TUG1表达。选择SKOV3细胞并分为si-TUG1组(转染TUG1 shRNA)和NC组(转染空载体质粒),采用CCK8、流式细胞术、划痕实验检测2组细胞增殖水平、细胞周期及细胞转移能力,Western blot检测2组蛋白激酶B(akt)、磷酸化哺乳动物雷帕霉素靶蛋白(mtor)、p-akt、p-mtor、细胞周期相关蛋白(Cyclin D1,Cyclin B1,CDK6)、转移相关蛋白(MMP-2,Snail)的相对表达量。结果RT-PCR检测结果显示,卵巢癌组织中TUG1表达高于癌旁组织(Pakt/akt、p-mtor/mtor、Cyclin D1、Cyclin B1、CDK6、MMP-2,Snail蛋白表达低于NC组(Pakt/mtor信号通路有关。

关键词：长链非编码RNA牛磺酸上调基因1 卵巢癌增殖 akt/mtor

Inhibitory effects of petasin on human colon carcinoma cells mediated by inactivation of akt/mtor pathway

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Chinese Medical Journal 2019年第9期132卷 1071-1078页

作者： Xi Lyu Ai-Lin Song Yin-Liang Bai Xiao-Dong Xu Dong-Qiang He You-Cheng Zhang The 5th Department of General Surgery Lanzhou University Second HospitalLanzhouGansu 730030China Department of Pharmacy Lanzhou University Second HospitalLanzhouGansu 730030China The 2nd Department of General Surgery Lanzhou University Second HospitalLanzhouGansu 730030China

Background:Colorectal cancer is the third most common cancer worldwide and still lack of effective therapy so ***,a natural product found in plants of the genus Petasites,has been reported to possess anticancer *** present study aimed to investigate the anticolon cancer activity of petasin both in vitro and in *** molecular mechanism of petasin was also further ***:Caco-2,LoVo,SW-620,and HT-29 cell lines were used to detect the inhibitory effect of petasin on colon cancer *** viability was determined using the MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide) *** apoptosis was analyzed by flow *** 33258 staining was used to visualize morphological *** migration was assessed using a wound-healing migration assay,and cell invasion was investigated using Transwell *** blotting assays were employed to evaluate the expression levels of proteins in the protein kinase B/mammalian target of rapamycin (akt/mtor) signaling ***,in vivo activity of petasin was evaluated using the SW-620 subcutaneous tumor model established in Balb/c nude *** rats were randomly divided into control group and 10 mg/kg petasin *** tumor volume was calculated every 7 days for 28 *** deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay was performed to assess the apoptotic effect of *** between two groups were assessed by analysis of independent-sample t ***:Petasin significantly inhibited the proliferation of human colon carcinoma cell lines,induced apoptosis,and suppressed migration and invasion in SW-620 *** blotting results showed that petasin decreased the phosphorylation of akt (1.01 ± 0.16 vs.0.74 ± 0.06,P = 0.042),mtor (0.71 ± 0.12 vs.0.32 ± 0.11,P = 0.013),and P70S6K (1.23 ± 0.21 vs.0.85 ± 0.14,P = 0.008),elevated the expression of caspase-3 (0.41 ± 0.09 vs.0.74 ± 0.12,P = 0.018) and caspas

关键词： Petasin Colon cancer Apoptosis Migration Invasion akt/mtor pathway

UBE2C affects breast cancer proliferation through the akt/mtor signaling pathway

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Chinese Medical Journal 2021年第20期134卷 2465-2474页

作者： Zi-Nan Lu Jia Song Tong-Hui Sun Gang Sun Department of Mammary/Head and Neck Surgery The Affiliated Tumor Hospital of Xinjiang Medical UniversityUrumqiXinjiang 830011China Department of Institute for Cancer Research The Affiliated Tumor Hospital of Xinjiang Medical UniversityUrumqiXinjiang 830011China

Background:Ubiquitin-conjugating enzyme E2C(UBE2C)has been shown to be associated with the occurrence of various cancers and involved in many tumorigenic *** study aimed to investigate the specific molecular mechanism through which UBE2C affects breast cancer(BC)***:BC-related datasets were screened according to filter criteria in the Gene Expression Omnibus(GEO)database and The Cancer Genome Atlas(TCGA)*** differentially expressed genes(DEGs)were identified using Venn diagram *** using DEGs,we conducted the following analyses including Gene ontology(GO),Kyoto Encyclopedia of Genes and Genomes(KEGG),protein-protein interaction(PPI),and survival analysis,and then validated the function of the hub geneUBE2C using quantitative reverse transcription-polymerase chain reaction(RT-qPCR),cell counting kit-8(CCK-8)assay,transwell assay,and Western blot ***:In total,151 DEGs were identified from the GEO and TCGA *** results of GO analysis demonstrated that the DEGs were significantly enriched with mitotic nuclear division,lipid droplet,and organic *** analysis showed that the peroxisome proliferators-activated receptor(PPAR)signaling pathway,regulation of lipolysis in adipocytes,and proximal tubule bicarbonate reclamation were significantly enriched in the signal transduction pathway *** top three hub genes that resulted from the PPI network wereFOXM1,UBE2C,*** results of survival analysis showed a close relationship between UBE2C and *** results of CCK-8 and transwell assays suggested that the proliferation and invasion ofUBE2C knockdown cells were significantly inhibited(Pakt),phosphorylated mammalian target of rapamycin(p-mtor),and hypoxia-in

关键词： akt/mtor Breast cancer Invasion Proliferation Ubiquitin-conjugating enzyme E2C

Zyxin promotes hepatocellular carcinoma progression via the activation of akt/mtor signaling pathway

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Oncology Research 2023年第5期31卷 805-817页

作者： TIANYING CAI JUNJIE BAI PENG TAN ZHIWEI HUANG CHEN LIU ZIMING WU YONGLANG CHENG TONGXI LI YIFAN CHEN JIAN RUAN LIN GAO YICHAO DU WENGUANG FU Department of Hepatobiliary Surgery Affiliated Hospital of Southwest Medical UniversityLuzhou646000China Biobank The Affiliated Hospital of Southwest Medical UniversityLuzhou646000China Academician(Expert)Workstation of Sichuan Province The Affiliated Hospital of Southwest Medical UniversityLuzhou646000China Department of Medical Oncology First Affiliated HospitalSchool of MedicineZhejiang UniversityHangzhou310000China Department of Health Management The Affiliated Hospital of Southwest Medical UniversityLuzhou646000China

Hepatocellular carcinoma(HCC)is a common malignancy that is driven by multiple genes and *** aim of this study was to investigate the role and specific mechanism of the actin-interacting protein zyxin(ZYX)in *** found that the expression of ZYX was significantly higher in HCC tissues compared to that in normal liver *** addition,overexpression of ZYX in hepatoma cell lines(PLC/PRF/5,HCCLM3)enhanced their proliferation,migration and invasion,whereas ZYX knockdown had the opposite effects(SK HEP-1,Huh-7).Furthermore,the change in the expression levels of ZYX also altered that of proteins related to cell cycle,migration and *** results were obtained with xenograft *** akt/mtor signaling pathway is one of the key mediators of cancer *** ZYX overexpression upregulated the levels of phosphorylated akt/mtor proteins,its knockdown had the opposite *** addition,the akt inhibitor MK2206 neutralized the pro-oncogenic effects of ZYX on the HCC cells,whereas the akt activator SC79 restored the proliferation,migration and invasion of HCC cells with ZYX *** together,ZYX promotes the malignant progression of HCC by activating akt/mtor signaling pathway,and is a potential therapeutic target in HCC.

关键词： Zyxin Hepatocellular carcinoma akt/mtor Proliferation Migration Invasion

How is the akt/mtor pathway involved in cell migration and invasion?

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BIOCELL 2023年第4期47卷 773-788页

作者： JINGYAO XU SHUANGLI HAO KAIYUE HAN WANXI YANG HONG DENG The Sperm Laboratory College of Life SciencesZhejiang UniversityHangzhou310058China Department of Pathology School of MedicineZhejiang UniversityHangzhou310058China

As a pathway that plays a role in nutrient absorption,anabolic response,cell growth and survival,the important role of akt/mtor in tumorigenesis has also come to *** cancer patients,most deaths are caused by the growth of metastatic tumors outside the primary ***,migration and invasion in the late stage of tumor progression are the main unresolved issues in the study of tumor pathogenesis,and akt/mtor has been found to participate in the migration and invasion of cancer cells,which means that the study of this pathway may contribute to a solution for the *** of its extensive and complex functions in the organism,this pathway can be regulated by a variety of different signals in the body,and then realize its function through different downstream signal *** article reviews the proteins that can indirectly affect this pathway by regulating the common upstream signaling molecules of this pathway,and the proteins that can directly affect the level of phosphorylation of akt/mtor in cancer *** also review the proteins that can co-regulate this pathway and its downstream *** this study,we hope to gain a deeper understanding of the regulatory mechanism of the akt/mtor pathway in cancer cells,in hopes of finding effective and harmless cancer treatment targets in the future.

关键词： akt/mtor Migration and invasion Cancer cell Signal pathway Regulation

akt／mtor信号通路在大鼠终板软骨细胞体外自然退变模型中的表达及意义

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中华医学杂志 2016年第5期96卷 375-379页

作者：张书丰王弘张涛徐宏光马明明张晓玲皖南医学院第一附属医院弋矶山医院脊柱外科安徽省芜湖市241000 中国科学院上海生命科学院上海交通大学健康科学研究所骨科细胞与分子生物学实验室

目的探讨akt／mtor信号通路在大鼠终板软骨细胞体外自然退变模型中的表达变化及其意义。方法分离、培养大鼠终板软骨细胞，建立大鼠终板软骨细胞体外自然传代退变模型。数字表法随机分为空白对照组（P2代细胞）、自然传代退变组（P5代... 详细信息

目的探讨akt／mtor信号通路在大鼠终板软骨细胞体外自然退变模型中的表达变化及其意义。方法分离、培养大鼠终板软骨细胞，建立大鼠终板软骨细胞体外自然传代退变模型。数字表法随机分为空白对照组（P2代细胞）、自然传代退变组（P5代细胞）、P5代akt／mtor信号通路抑制剂组、P5代akt／mtor信号通路激动剂组。倒置相差显微镜观察各组细胞的形态；甲苯胺蓝染色检测各组细胞蛋白聚糖的变化；免疫印迹法检测akt及P—akt蛋白的表达变化；实时聚合酶链反应检测各组细胞中Ⅱ型胶原、蛋白聚糖、SOX9及akt／mtor信号通路中的关键基因mtor基因表达变化。结果随着大鼠终板软骨细胞的体外自然传代退变的进行，大鼠终板软骨细胞的表型逐渐减少甚至丢失；在自然传代组中：Ⅱ型胶原（P5／P2=0．28，P=0．0427）、蛋白多糖（P5／P2=0．33，P=0．0263）、SOX9（P5／P2=0．40，P：0．0182）及mtor（P5／P2=0．28，P=0．0381）的表达明显降低；在akt／mtor抑制剂组中：Ⅱ型胶原（P5／P2=0．19，P=0．0347）、蛋白多糖（PS／P2=0．25，P=0．023）、SOX9（P5／P2=0．31，P=0．0342）及mtor（P5／P2=0．20，P=0．0241）的表达较自然传代组降低；在akt／mtor激动剂组中：及Ⅱ型胶原（P5／P2=0．41，P=0．0441）、蛋白多糖（P5／P2=0．53，P=0．0151）、SOX9（P5／P2=0．61．P=0．0197）roTOR（PS／P2=0．41，P=0．0381）的表达较自然传代退变及抑制剂组升高。结论akt／mtor信号通路可能在大鼠终板软骨细胞体外自然传代退变的过程中有具有十分重要的作用，人为添加akt／mtor信号通路的抑制剂（LY294002）或激动剂（IGF-1）可加速或抑制、减缓大鼠终板软骨细胞体外退变的发生。

关键词：椎间盘软骨细胞信号传递细胞衰老 akt/mtor